The long term objective of this proposal is to determine how patency of the pharyngeal airway is controlled in sleeping premature infants. The pharynx contributes 80% of supraglottic resistance in the supine infant and is most vulnerable to collapse during apnea. We hypothesize that the infant's ability to maintain patency of the pharynx is inadequately developed when the baby is born prematurely. We propose that pharyngeal airway resistance is largely determined by the passive mechanical properties of the airway wall and by intraluminal pressure. Support of the airway by contraction of dilating muscles such as the genioglossus is not expected to occur until a high threshold of chemoreceptor or mechanoreceptor input to the medulla is achieved. The studies in this proposal which will be performed in unsedated premature infants will examine the way in which conditions such as change in posture, increased chemoreceptor input, resistive loading, lung volume and postnatal growth alter resistance in the pharyngeal airway. The contribution of a representative pharyngeal dilator, the genioglossus, to change in airway resistance will be evaluated via surface EMG activity. Additional studies will investigate alteration in pharyngeal stability in apneic infants, and the mechanism of action of theophylline in obstructive apnea. We will explore the hypothesis that increased resistance in the pharynx may contribute to the pathophysiology of two diseases (1) a form of chronic lung disease in infants, bronchopulmonary dysplasia and (2) respiratory syncytial virus. Results will form the basis of a model of mechanical properties of the pharynx which will describe the contribution of this part of the airway to overall pulmonary function. The studies in this proposal will provide new information on the forces which control pharyngeal patency in premature infants as well as insight into the vulnerability of this part of the airway in acute and chronic lung disease of infancy.